Nuclear pore complexes (NPCs) mediate communication between the nucleus and the cytoplasm, and regulate gene expression by interacting with transcription and mRNA export factors. Lysine acetyltransferases (KATs) promote transcription through acetylation of chromatin-associated proteins. We find that Esa1, the KAT subunit of the yeast NuA4 complex, also acetylates the nuclear pore basket component Nup60 to promote mRNA export. Acetylation of Nup60 recruits the mRNA export factor Sac3, the scaffolding subunit of the Transcription and Export 2 (TREX-2) complex, to the nuclear basket. The Esa1-mediated nuclear export of mRNAs in turn promotes entry into S phase, which is inhibited by the Hos3 deacetylase in G1 daughter cells to restrain their premature commitment to a new cell division cycle. This mechanism is not only limited to G1/S-expressed genes but also inhibits the expression of the nutrient-regulated GAL1 gene specifically in daughter cells. Overall, these results reveal how acetylation can contribute to the functional plasticity of NPCs in mother and daughter yeast cells. In addition, our work demonstrates dual gene expression regulation by the evolutionarily conserved NuA4 complex, at the level of transcription and at the stage of mRNA export by modifying the nucleoplasmic entrance to nuclear pores.

中文翻译：

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核孔复合物乙酰化调节芽殖酵母中的 mRNA 输出和细胞周期承诺


核孔复合物 (NPC) 介导细胞核和细胞质之间的通讯，并通过与转录和 mRNA 输出因子相互作用来调节基因表达。赖氨酸乙酰转移酶 (KAT) 通过染色质相关蛋白的乙酰化来促进转录。我们发现酵母 NuA4 复合物的 KAT 亚基 Esa1 也乙酰化核孔篮成分 Nup60 以促进 mRNA 输出。 Nup60 的乙酰化将 mRNA 输出因子 Sac3（转录和输出 2 (TREX-2) 复合物的支架亚基）招募到核篮。 Esa1 介导的 mRNA 核输出反过来促进进入 S 期，该阶段受到 G1 子细胞中 Hos3 脱乙酰酶的抑制，以抑制其过早进入新的细胞分裂周期。这种机制不仅限于G1/S表达的基因，而且还特异地抑制子细胞中营养调节的GAL1基因的表达。总的来说，这些结果揭示了乙酰化如何促进母酵母细胞和子酵母细胞中 NPC 的功能可塑性。此外，我们的工作证明了进化上保守的 NuA4 复合物在转录水平和 mRNA 输出阶段通过修饰核孔的核质入口进行双重基因表达调控。